Common Lambsquarters (Chenopodium album) is a dicot weed in the Chenopodiaceae family. In Quebec this weed first evolved resistance to Group B/2 herbicides in 2008 and infests Soybean. Group B/2 herbicides are known as ALS inhibitors (Inhibition of acetolactate synthase ALS (acetohydroxyacid synthase AHAS)). Research has shown that these particular biotypes are resistant to thifensulfuron-methyl and they may be cross-resistant to other Group B/2 herbicides.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

Greenhouse trials comparing a known susceptible Common Lambsquarters biotype with this Common Lambsquarters biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group B/2 resistant Common Lambsquarters have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group B/2 resistant Common Lambsquarters from Quebec please update the database.

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Quebec have been instrumental in providing you this information. Particular thanks is given to Francois Tardif for providing detailed information.

Thiel, H. ; Varrelmann, M.. 2014.
Identification of a new PSII target site psbA mutation leading to D1 amino acid Leu218Val exchange in the Chenopodium album D1 protein and comparison to cross-resistance profiles of known modifications at positions 251 and 264.
Pest Management Science70
:
278 - 285.

BACKGROUND: Resistance of Chenopodium album to triazinones and triazines can be caused by two amino acid exchanges, serine-264-glycine (Ser264Gly) and alanine-251-valine (Ala251Val), in the chloroplast D1 protein. This paper describes the identification of a biotype with a leucine-218-valine (Leu218Val) switch found in German sugar beet fields with unsatisfactory weed control. A greenhouse experiment has been performed to compare the resistance profile of the newly identified biotype with biotypes that carry the Ser264Gly and Ala251Val mutations. RESULTS: Application rate-response curves obtained from the greenhouse experiment showed that the Leu218Val exchange induced significant resistance against the triazinones but not against terbuthylazine. The level of resistance against the triazinones was higher in the Ser264Gly and Ala251Val biotypes compared with the Leu218Val biotype. All biotypes tested were more resistant to metribuzin than to metamitron. Following terbuthylazine treatment, Ser264Gly displayed a high level of resistance, Ala251Val showed moderate resistance. A PCR-RFLP assay for Ser264Gly has been extended to include detection of Ala251Val and Leu218Val mutations. CONCLUSION: The D1 Leu218Val substitution in C. album confers significant resistance to triazinones. This suggests that Leu218Val is involved in the binding of triazinones. First establishment of the resistance profiles of the three psbA mutations suggests that these mutations have been independently selected..

Tracing spread of weeds with molecular markers can give valuable information on the importance of migration mechanisms. This study investigated the local spread of metamitron-resistant Chenopodium album patches in the west of the province West Flanders (Belgium) using amplified fragment length polymorphism (AFLP) markers. During the summer of 2009, leaf samples of C. album plants were harvested in 27 patches, distributed over 10 sugar beet fields and one maize field. The fields were grouped in four local clusters, each corresponding to a farmer who cultivated these fields. A cleaved amplified polymorphic sequence procedure identified the Ser264 to Gly mutation in the D1 protein, endowing resistance to metamitron, a key herbicide applied in sugar beet. The majority of the sampled plants within a patch (97% on average) carried this mutation. Genetic variation among the four farmers' locations (12%) and among the C. album patches within the farmers' locations (14%) was significant according to amova (P<0.001). In addition, Mantel tests confirmed a positive correlation between genetic distance (linearised φPT between pairs of patches) and the logarithm of geographic distance for the complete data set (Mantel coefficient significant at P=0.001), suggesting isolation by distance. Nevertheless, genetic similarity between patches from different fields indicated that seed transport by agricultural machinery and manure is likely to have an important impact on the spread of metamitron-resistant biotypes. Farmers should become aware of the resistance problem as soon as possible, in order to prevent further spread in their fields..

BACKGROUND: In recent years, common lambsquarters (Chenopodium album L.) populations from sugar beet fields in different European countries have responded as resistant to the as-triazinone metamitron. The populations have been found to have the same D1 point mutation as known for atrazine-resistant biotypes (Ser264 to Gly). However, pot experiments revealed that metamitron resistance is not as clear-cut as observed with triazine resistance in the past. The objectives of this study were to clarify the absorption, translocation and metabolic fate of metamitron in C. album. RESULTS: Root absorption and foliar absorption experiments showed minor differences in absorption, translocation and metabolism of metamitron between the susceptible and resistant C. album populations. A rapid metabolism in the C. album populations was observed when metamitron was absorbed by the roots. The primary products of metamitron metabolism were identified as deamino-metamitron and metamitron-N-glucoside. PABA, known to inhibit the deamination of metribuzin, did not alter the metabolism of metamitron, and nor did the cytochrome P450 inhibitor PBO. However, inhibition of metamitron metabolism in the presence of the cytochrome P450 inhibitor ABT was demonstrated. CONCLUSION: Metamitron metabolism in C. album may act as a basic tolerance mechanism, which can be important in circumstances favouring this degradation pathway..

Chenopodium albumL. is a major weed in spring-planted crops in the temperate regions of the world. Since 2000, farmers have reported an unsatisfactory control of this weed in sugar beet fields in Belgium, France and The Netherlands. Frequently, the survivingC. albumplants are resistant to metamitron, a key herbicide in this crop. Metamitron resistance inC. albumis caused by a Ser264 to Gly mutation in the psbA gene on the chloroplast genome, which prevents binding of metamitron to its target site. This mutation causes also resistance to other herbicides with a similar mode of action, like metribuzin -applied in potato- and atrazine in particular. Atrazine has been applied very frequently in maize in the 1970s and the 1980s, but is now banned in Europe due to environmental reasons. The persistent use of atrazine in maize confronted Belgian and other European farmers in the early 1980s with atrazine resistantC. albumwith the same Ser264 to Gly mutation. The problems with atrazine resistantC. albumdisappeared when other herbicides were applied in maize. Unfortunately, this is not the case for metamitron resistantC. albumin sugar beet, because no replacement herbicide is readily available. The history of atrazine use in maize brought up a question concerning the origin of the current metamitron resistantC. albumpopulations. Have these populations been selected locally by regular use of metamitron in sugar beet or did the selection occur earlier by atrazine use when maize was grown in the same fields? This would have serious implications regarding the reversibility of herbicide resistance. Therefore, soil samples were collected on 16 fields with different histories: five fields with an organic management over 25 years, two fields with a history of atrazine resistantC. album, five fields with metamitron resistantC. albumin sugar beet and four fields which were under permanent grassland for 10 years, preceded by a regular rotation in which sugar beet was a key crop. The seeds ofC. albumwere extracted from the soil and germinated on a germination table. Germinated seeds were allowed to grow in a growth chamber. Metamitron resistance was determined by a chlorophyll fluorescence test and leaf material was sampled for AFLP-analysis. For all fields, estimations were made of the size of the seed bank (i.e. an indirect estimate of population size), the frequency of resistant plants and the genetic diversity of resistant and susceptible populations. The results indicate that herbicide-resistant C. album populations are persistent and maintain their adaptive capacity, challenging future management of metamitron resistantC. album.

Agrikola, Y. ; Petersen, J.. 2012.
Importance and approaches for the control of different photosystem-II-inhibitor resistant Chenopodium album biotypes in sugar beet and potatoes.
Julius-Kühn-Archiv1
:
111 - 118.

Resistance in weeds to PS-II herbicides is well known. From the end of the 1970s resistance to triazines in maize represented a particular problem. Today, because of the variety of alternative active ingredients for use on maize, this problem is considered to be solved. This is different for sugarbeet and potatoes because hardly any new herbicides have been developed during the last 20 years. Chenopodium album is a major weed in all summer crops. In maize, resistance to triazines (target-site resistance (TSR) at position 264 on the D1 protein) is known. In recent years, new TSRs in C. album (position 251 in Sweden and 218 in Lower Saxony, Germany) have been found. These biotypes exhibit resistance to triazinones and chloridazon but showed no cross-resistances to triazines. An outdoor pot trial with sugarbeet and potatoes showed that higher dosages of ethofumesate in sugarbeet and aclonifen in potatoes are able to control triazine- and triazinone-resistant C. album biotypes to a certain extent or even completely, respectively. A competition pot trial with maize and different C. album biotypes showed no significant differences in weed fitness concerning the parameters plant height, biomass and seed production..